IS THERE A FUTURE FOR ANTIARRHYTHMIC DRUG-THERAPY

Citation
Pg. Guerra et al., IS THERE A FUTURE FOR ANTIARRHYTHMIC DRUG-THERAPY, Drugs, 56(5), 1998, pp. 767-781
Citations number
157
Categorie Soggetti
Pharmacology & Pharmacy",Toxicology
Journal title
DrugsACNP
ISSN journal
00126667
Volume
56
Issue
5
Year of publication
1998
Pages
767 - 781
Database
ISI
SICI code
0012-6667(1998)56:5<767:ITAFFA>2.0.ZU;2-I
Abstract
Drug therapy has traditionally been the mainstay of treatment for both ventricular and supraventricular arrhythmias. However, increasing kno wledge about the potentially significant adverse effects of these medi cations, together with the emergence of new, nonpharmacological approa ches to the treatment of arrhythmias, has led some to question the fut ure of antiarrhythmic drug therapy. Antiarrhythmic drugs are quite eff ective in terminating a variety of arrhythmias, including atrioventric ular (AV) node re-entrant and AV tachycardias (particularly calcium an tagonists and adenosine), atrial flutter (class III agents) and atrial fibrillation (class IA and IC drugs. The chronic use of antiarrhythmi c drugs has been increasingly limited by a fear of adverse effects (es pecially proarrhythmia) and the availability of highly effective nonph armacological alternatives (particularly ablation for re-entrant tachy cardias involving the AV node and bypass tracts and cardiovertor/defib rillators for malignant ventricular arrhythmias. Atrial fibrillation ( AF) continues to be a therapeutic challenge for which there is no safe and curative nonpharmacological therapy. Antiarrhythmic drugs of clas ses IA, IC and III show efficacy in preventing recurrence of AF but th ere are concerns about possible pro-arrhythmic complications. In the f uture, antiarrhythmic agents will continue to be used acutely to termi nate a broad range of sustained arrhythmias. Chronic use is likely to depend on the development of safer and/or more effective compounds, as well as on improved ways of predicting which patients are likely to d evelop pro-arrhythmic reactions. The development of molecular electrop hysiology will allow for the identification of agents with selected io n channel blocking profiles which may prove efficacious with a lower r isk of complications. Finally, an improved understanding of arrhythmia substrates may permit the identification of therapy that prevents arr hythmias by acting on the underlying substrate, rather than simply try ing to modify the electrical end product.